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Ischemic stroke exhibits characteristics of higher morbidity, mortality and disability. The spatial-temporal evolution of ischemic stroke is complex, and the traditional histopathological analysis has the inherent limitation of not allowing real-time and dynamic monitor examination. Magnetic resonance imaging (MRI) is able to real-time and dynamic monitor the evolution of ischemic damage. In our study, MRI and histopathological analysis were combined to track lesion progression both functionally and structurally.
Rat model of stroke was induced by permanent middle cerebral artery occlusion (pMCAO). MRI was performed at 3,7,14 and 30 days. T2WI and T2 mapping were performed to evaluate the evolutional changes of infraction and post-ischemia cerebral edema, respectively. Magnetic resonance angiography (MRA) images were used to perform the morphological alterations of main and accessory middle cerebral artery. Cerebral blood flow (CBF) was determined by continuous arterial spin labeling. In addition, proton magnetic resonance spectroscopy (1HMRS) was applied to evaluate the abnormalities in various neurochemical metabolites, including N-acetyl aspartate (NAA), Choline (Cho) and creatine (Cr). Moreover, at last time point, transmission electron microscopy (TEM), combined with hematoxylin-eosin (HE) staining was performed to evaluate pathological changes after ischemic stroke.
The cerebral infraction volume was gradually reduced from 3 to 30 days in stroke group. At 3 and 7days, the brains showed edema in stroke group, evidenced by a pronounced midline shift. The T2 values, obtained by T2 mapping sequence were used to evaluate post-ischemia cerebral edema, were significantly increased in stroke group at all time points. Middle cerebral artery occlusion was observed in all pMCAO rats. Vascular signal intensity and cerebral blood flow were significantly decreased after ischemic stroke. The NAA/Cr ratio was significantly reduced in the subacute phase (3 – 7 days) after stroke, followed by spontaneous recovery to normal level at 14 day after ischemia. The Cho/Cr ratio was obviously increased from 3 to 14 days. TEM and HE displayed remarkable pathological changes, including neuron necrosis, swollen of astrocytes and capillaries.
The temporal evolution of ischemic damage in vivo can be sensitively and specifically detected with the application of MRI. MRI could be better to display post-ischemia changes in cerebral edema, cerebrovascular, cerebral blood flow, and neurochemical metabolism. After ischemic stroke, the reduced focal blood flow leads to injury cascade, such as edema, apoptosis of nerve cells and neurochemical metabolic disorders at all stage of stroke.